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Coronary Artery Calcification and Family History of Myocardial Infarction in the Dallas Heart Study
Study Questions:
What is the association of family history of myocardial infarction (MI) and coronary artery calcification (CAC) with incident coronary heart disease (CHD)?
Methods:
Data from the Dallas Heart Study were used for the present study. Participants without cardiovascular disease at baseline and who had prevalent CAC by electron-beam computed tomography were included. Family history of MI was defined as having a first-degree relative with an MI. The primary outcome of interest was a composite of CHD-related death, MI, and percutaneous or surgical coronary revascularization. Mean follow-up was 8.0 ± 1.2 years. In addition, the individual and joint associations with the CHD composite outcome were determined for family history of MI and CAC.
Results:
A total of 2,390 participants were included. The mean age of the population was 44 ± 9 years and 56% were female. Almost half were African American (48%) and approximately one-third had a family history of MI (32%). A CAC score of 0 was observed in 47% of the cohort. Participants with a positive family history of MI tended to be older, were more often female, had higher prevalence of hypertension and diabetes, and had a more unfavorable lipid profile. A total of 76 first CHD events occurred over a mean follow-up of 8 ± 1.2 years (including 17 CHD-related deaths, 38 nonfatal MIs, 16 percutaneous coronary revascularizations, and 5 coronary bypass surgeries). Coronary event rates in those with both a family history of MI and CAC were 8.8% versus 3.3% in those with prevalent CAC alone (p < 0.001). Among those without CAC, CHD rates were 1.9% in those with a family history of MI compared with 0.4% in those without a family history of MI (p < 0.017). In multivariate models adjusted for traditional risk factors, a family history of MI was independently associated with CHD (adjusted hazard ratio [HR], 2.6; 95% confidence interval [CI], 1.6-4.2; p < 0.001). Further adjustment for prevalent CAC did not diminish this association (HR, 2.6; 95% CI, 1.6-4.2; p < 0.001). Family history of MI and CAC appeared to be additive. CHD event rates in those with both a family history of MI and CAC were 8.8% vs. 3.3% in those with prevalent CAC alone. CHD rates were 1.9% in those with a family history of MI alone compared with 0.4% in those with neither a family history of MI nor CAC. Among subjects without CAC, a family history of MI characterized a group with a more unfavorable cardiometabolic profile.
Conclusions:
The investigators concluded that family history of MI provided prognostic information that was independent of and additive to CAC. Among those with CAC, family history of MI identified subjects at particularly high short-term risk, and, among those without family history of MI, selected a group with an adverse risk-factor profile.
Perspective:
It is not clear why the traditional definition of premature family history of CHD was not used in this analysis, as opposed to a family history of any MI (which was used). It appears that participants with a family history of any MI were older and had a more unfavorable metabolic profile. Reproducing these findings in larger cohorts which use a definition of premature family history is warranted. Providers should continue to ask about family history, in particular, a history of premature CHD, along with assessment of cardiometabolic profile in the assessment of risk.
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